Expression of Catechol O methyl transferase (COMT) with the contrasting effects of 17β estradiol (E2): Implications for the mechanism of estrogen-induced ovarian carcinogenesis.

Background: Epidemiological data show that induction of ovarian cancer is related to estrogen exposure and metabolism. In addition catechol metabolites of estrogen also contribute to carcinogenesis. O methylation by Catechol O methyl transferase (COMT) is a phase II metabolic inactivation pathway for catechol estrogens. The goal of the present study was to investigate the role of COMT level in ovarian carcinogenesis with the contrasting effects of 17 β estradiol level. Subjects and methods Our study was conducted on 80 subjects divided into 30 patients with malignant ovarian tumors ,30 patients with benign ovarian tumors and 20 healthy controls. Tissue and serum levels of COMT and 17 17 β estradiol were determined using ELISA Results According to our results COMT inhibition in the malignant group was detected as high as 7.1 pmol/L E2 in serum and 15.6 pmol/L E2 in tissue homogenate. This inhibition was absent in the benign group as high as 7.53 pmol/L E2 in serum and as high as 14.9 pmol/L E2 in tissue homogenates. Conclusions Our results provide evidence for the protective effect of COMT in benign ovaries against neoplastic transformation. This supports the notion that targeting the metabolism of estrogen can be an another way to reduce ovarian cancer risk.